Inflammation promotes a cytokine response and disrupts the cervical epithelial barrier: a possible mechanism of premature cervical remodeling and preterm birth

Abstract

Objective: An inflammatory challenge disrupts the cervical epithelial barrier and promotes cervical remodeling.

Study design: Immortalized ectocervical and endocervical cells were treated with lipopolysaccharide (LPS), and interleukin (IL)-6, IL-8, and soluble E-cadherin (SECAD) were assessed. Cells were then pretreated with dexamethasone prior to LPS exposure, and IL-6, IL-8, and SECAD levels were again assessed. The integrity of the epithelial cell barrier was determined using a permeability assay.

Results: LPS significantly increased IL-6 and IL-8 levels, and SECAD was significantly increased at 24 hours. LPS induced inflammation increased permeability for both cell lines. Dexamethasone pretreatment prior to LPS exposure significantly decreased IL-6 and IL-8 levels in both cell lines. There was no reduction in SECAD levels with dexamethasone pretreatment. Permeability decreased in the presence of dexamethasone for ectocervical cells only.

Conclusion: These studies demonstrate an inflammatory challenge to cervical epithelial cells promotes a cytokine release and functionally alters the cervical epithelial barrier.